Bickerstaff’s brainstem encephalitis, Miller Fisher syndrome and Guillain-Barré syndrome overlap in an asthma patient with negative anti-ganglioside antibodies

BMC Research Notes

Yong-Xin Sun³  Jia Xu²  Wei Sun³  Yuchuan Ding¹  Vance Fredrickson¹  Xunming Ji³  Jianping Jia³  Yuan Wang³  Chongyu Han² 

[1] Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, MI, 48201, USA;Department of Neurology, You Anmen Hospital, 100069, Beijing, People's Republic of China;Department of Neurology, Xuan Wu Hospital of Capital Medical University, 100053, Beijing, People's Republic of China

关键词: Guillain-Barré syndrome;    Miller Fisher syndrome;    Bickerstaff’s brainstem encephalitis;    Autoimmune;    Asthma;   

Others  :  1166305
DOI  :  10.1186/1756-0500-5-295

 received in 2012-04-09, accepted in 2012-06-14,  发布年份 2012

【 摘 要 】

Background

Bickerstaff’s brainstem encephalitis (BBE), together with Miller Fisher syndrome (MFS) and Guillain-Barré syndrome (GBS) were considered to form a continuous clinical spectrum. An anti-GQ1b antibody syndrome has been proposed to underlie the common pathophysiology for the three disorders; however, other studies have found a positive anti-GM1 instead of anti-GQ1b antibody.

Case presentation

Here we report a 20-year-old male patient with overlapping BBE, MFS and GBS. The patient had a positive family history of bronchial asthma and had suffered from the condition for over 15 years. He developed BBE symptoms nine days after an asthma exacerbation. During the course of illness, he had significantly elevated IgE levels in both serum and cerebrospinal fluid. Serologic analysis of antibodies against ganglioside complexes (anti-GDIa, anti-GDIb, anti-GM1, anti-GM2, anti-GM3, anti-GQIb and anti-GTIb antibodies) showed negative results.

Conclusions

Since asthma has recently been related to autoimmune disease, our case supports an autoimmune mechanism underlying the clinical spectrum composed of BBE, MFS and GBS. However, contrary to a proposed anti-GQ1b antibody syndrome, we would suggest that pathogenesis of this clinical spectrum is not limited to anti-ganglioside antibodies.

【 授权许可】

   
2012 Chongyu et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

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